Biogenic Nanoselenium Particles Effectively Attenuate Oxidative Stress-Induced Intestinal Epithelial Barrier Injury by Activating the Nrf2 Antioxidant Pathway

In
the present study, a new form of selenium nanoparticle (biogenic nanoselenium
(BNS) particles) was synthesized using bacteria. The protection of
BNS particles against oxidative stress-induced intestinal barrier
dysfunction and the inherent mechanisms of this process were investigated,
and selenomethionine (SeMet) and chemically synthesized nanoselenium
(Nano-Se) particles were used for comparison. Characterization of
BNS particles revealed that they were monodispersed and homogeneous
spheres, with an average size of 139.43 ± 7.44 nm. In the mouse
model of intestinal oxidative stress, BNS particles were found to
protect the mouse intestinal barrier function and preserve intestinal
redox homeostasis more efficiently than SeMet and Nano-Se. In vitro
experiments with porcine jejunum epithelial (IPEC-J2) cells verified
the stronger epithelial barrier-protecting effect of BNS particles
against oxidative stress, with reduced cell apoptosis and an improved
cell redox state. BNS activated the nuclear factor (erythroid-derived-2)-like
2 (Nrf2) and increased the expression of its downstream genes, including
thioredoxin reductase (TXNRD)-1, NADPH dehydrogenase (NQO)-1, heme
oxygenase (HO)-1, and thioredoxin (Trx), in dose- and time-dependent
manners. In contrast, SeMet and Nano-Se merely enhanced the activity
of the selenoenzymes TXNRD-1 and glutathione peroxidase (GPx)-1, indicating
the role of selenium donors. Moreover, the knock down of Nrf2 significantly
blocked the antioxidative effect of BNS, confirming that BNS protects
the intestinal barrier from oxidative stress-induced damage by activating
Nrf2 and its downstream genes. Our results suggest that BNS is a promising
selenium species with potential application in treating oxidative
stress-related intestinal diseases.